Jenny Hyde, PhD
8447 Riverside Pkwy
Medical Research Education Building, Room 234
Bryan, TX 77807-3260
Education and Post-Graduate Training
BS, Microbiology, Texas A&M University (2000)
PhD, Texas A&M Health Science Center (2005)
Postdoctoral Fellow, Texas A&M Health Science Center (2005-2010)
Borrelia burgdorferi, the spirochetal bacterium that causes Lyme disease, is the most common tick-borne infection in the United States with over 35,198 cases reported in 2008. This value represented a 28 percent and 77 percent increase in incidence in the previous two years of reporting, respectively, indicating that Lyme borreliosis is a re-emerging disease. Early on, the infection is characterized by a skin lesion known as erythema migrans and a non-descript flu-like illness. Patients with untreated Lyme disease experience multisystemic symptoms with the arthritis being the defining indicator of long-term untreated infection.
The long-term objective of my research is to identify and characterized virulence determinants that contribute to the pathogenic potential of the B. burgdorferi. Through the utilization of in vivo bioluminescence we are evaluating the kinetics of borrelial infectivity in various strains or mutant derivatives that exhibit distinct phenotypes. We are also tracking how in vivo synthesis of critical virulence determinants affects B. burgdorferi colonization and dissemination. This work will contribute to the current body of knowledge by shedding light on the pathogenic and temporal role of specific borrelial genes during the infectious process.
- Hyde JA (2017) Borrelia burgdorferi keeps moving and carries on: A review on borrelial dissemination and invasion. Frontiers in Immunology 8:114. doi: 10.3389/fimmu.2017.00114.
- Ramsey, M.E., Hyde, J.A., Medina-Perez, D.N., Lin, T., Gao, L., Lundt, M.E., Li, X., Norris, S.J., Skare, J. T., and L. Hu. 2017. A high-throughput genetic screen identifies previously uncharacterized Borrelia burgdorferi genes important for resistance against reactive oxygen and nitrogen species. PLoS Pathog. 13(2):e1006225
- Skare JT, Shaw DK, Trzeciakowski JP, Hyde JA (2016) In Vivo imaging demonstrates that Borrelia burgdorferi ospC is uniquely expressed temporally and spatially throughout experimental infection. PLoS ONE 11(9): e0162501. doi: 10.1371/journal.pone.0162501
- Hui Zhi, E.H. Weening, E.M. Barbu, J.A. Hyde, M. Höök, and J.T. Skare. 2015. The Borrelia burgdorferi BBA33 lipoprotein recognizes collagen and vitronectin and is essential for borrelial pathogenesis. Mol. Microbiol. 96(1):68-83.
- R.D. Gilmore, Brandt K.S. and J.A. Hyde. 2014. B. burgdorferi pncA and bptA are insufficient to maintain Ixodes colonization and persistence in lp25 deficient background. Infect. Immun. 82(12) PMID:25245809
- Shaw, D. K., Hyde, J. A., and J. T. Skare. 2011. The Borrelia burgdorferi BB0646 protein is responsible for the lipase and hemolytic activity associated with the aetiological agent of Lyme disease. Mol. Microbiol. 83(2):319-334.
- Hyde, J.A., Weening, E.H., Chang, M.H., Höök, M., Cirrillo, J.D., and J. T. Skare. 2011. Bioluminescent imaging of Borrelia burgdorferi in vivo demonstrates that the fibronectin-binding protein BBK32 is required for optimal infectivity. Mol. Microbiol. 82(1):99-113.
- Hyde, J.A., Weening, E.H., and J. T. Skare. 2011. Genetic Transformation of Borrelia burgdorferi. Curr Protoc Microbiol. Unit 12C.4.1-17.
- Hyde, J.A., Shaw, D.K., Smith, R., Trzeciakowski, J.P., and J. T. Skare. 2010. Characterization of a Conditional bosR Mutant in Borrelia burgdorferi. Infect. Immun. 78(1): 265-274***. PMID: 19858309
***Featured as a “Spotlight” Article in the January 2010 issue
- Hyde, J.A., Shaw, D.K., Smith, R., Trzeciakowski, J.P., and J. T. Skare. 2009. The BosR regulatory protein of Borrelia burgdorferi interfaces with the RpoS regulatory pathway and modulates both the oxidative
stress response and pathogenic properties of the Lyme disease spirochete. Mol Microbiol. 74(6): 1344-1355**. PMID: 19906179
**A MicroCommentary accompanied this article
- Hyde, J. A., Trzeciakowski, J. P. and J. T. Skare. 2007. Borrelia burgdorferi Alters its Gene Expression and Antigenic Profile in Response to CO2 Levels. J. Bacteriol. 189(2): 437-445. PMID: 17098904
- Hyde, J. A., Seshu, J. and J. T. Skare. 2006. Transcriptional Profiling of Borrelia burgdorferi Containing a Unique bosR Allele Identifies a Putative Oxidative Stress Regulon. Microbiology 152(9): 2599-2609. PMID: 16946255
- Seshu, J., Boylan, J. A., Hyde, J. A., Swingle, K. L., Gherardini, F. C. and J. T. Skare. 2004. A Conservative Amino Acid Change Alters the Regulatory Activity of BosR, the Redox Regulator of Borrelia burgdorferi. Mol. Microbiol. 54(5): 1352-1363. PMID: 15554974